期刊
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
卷 99, 期 -, 页码 55-64出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semedb.2018.05.005
关键词
Neurodegeneration; Network biology; Protein-protein interaction; Pathobiology; Interactome
资金
- Academy of Finland [296409]
- Finnish Cultural Foundation
- Academy of Finland (AKA) [296409, 296409] Funding Source: Academy of Finland (AKA)
alpha-synuclein and Tau are proteins prone to pathological misfolding and aggregation that are normally found in the presynaptic and axonal compartments of neurons. Misfolding initiates a homooligomerization and aggregation cascade culminating in cerebral accumulation of aggregated alpha-synuclein and Tau in insoluble protein inclusions in multiple neurodegenerative diseases. Traditionally, alpha-synuclein-containing Lewy bodies have been associated with Parkinson's disease and Tau-containing neurofibrillary tangles with Alzheimer's disease and various frontotemporal dementia syndromes. However, there is significant overlap and co-occurrence of alpha-synuclein and Tau pathologies in a spectrum of neurodegenerative diseases. Importantly, alpha-synuclein and Tau can interact in cells, and their pathological conformations are capable of templating further misfolding and aggregation of each other. They also share a number of protein interactors indicating that network perturbations may contribute to chronic proteotoxic stress and neuronal dysfunction in synucleinopathies and tauopathies, some of which share similarities in both neuropathological and clinical manifestations. In this review, we focus on the protein interactions of these two pathologically important proteins and consider a network biology perspective towards neurodegenerative diseases. (C) 2018 Elsevier Ltd. All rights reserved.
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